Pregnancy-induced hypertension (PIH) is associated with increased fetal and neonatal morbidity and mortality possibly resulting from hypoxia in utero. The primary pathology of PIH involves a reduction in uteroplacental blood flow but modern imaging techiques have now shown that increased impedance of the fetal- placental circulation and hence reduced blood flow can also be found in PIH. This may represent a direct effect of hypoxia or be a fetal adaptation to increase placental oxygen extraction to relieve hypoxia. The fetal-placental circulation is regulated by humoral agents and vascular pressure. An imbalance of vasodilator prostacyclin (PGI2) and vasoconstrictor thromboxane (TxA2) production is reported to underlie the vasoconstriction seen in PIH. We will commence with the premise that there is an imbalance of PGI2 and TxA2 in PIH. We will establish in the fetal-placental circulation of the perfused human placental cotyledon from both normotensive and PIH pregnancies: 1. If such an imbalance in PGI2/TxA2 production exists 2. Its relationship to the responses of the fetal-placental circulation to vasoconstrictors 3. The effect of increasing fetal-placental flow on PGI2 production and responses to vasoconstrictors. 4. The effects of hypocalcemia and hypomagnesemia on PGI2 synthesis and if supplementation with these cations alters responses to vasoconstrictors 5. If hypoxia reduces PGI2 synthesis or angiotensin converting enzyme activity and so alters vascular reactivity 6. Whether there is an increase in lipoxygenase product (leukotriene) formation linked to the deficiency in PGI2 synthesis 7. If drugs now used to restore the PGI2/TxA2 balance in PIH may cross the placenta and alter umbilical vascular reactivity. Our primary objective is to elucidate the potential role an imbalance in PGI2/TxA2 may have in controlling the vascular reactivity of the fetal/placental circulation, what the underlying mechanisms are behind the PGI2/TxA2 imbalance and how therapeutic agents may affect this to improve blood flow and reduce fetal morbidity and mortality.